Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0011881 (diabetic nephropathy)
10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Proteinuria in diabetes is associated with progressive glomerular damage. We studied the effects of 3-wk dietary protein restriction on proteinuria and renal function in 10 insulin-dependent diabetic men with diabetic nephropathy. Patients were randomly assigned by a crossover design to 40-g low-protein diet (LPD) or usual-protein diet (UPD). Glomerular filtration rate and renal plasma flow were measured by inulin and p-aminohippurate clearance at the end of each period under conditions of sustained euglycemia. Total calorie intake, body weight, serum albumin and total protein concentrations, hematocrit, blood pressure, and glucose control were similar during the two diets. Achieved protein intake was 46 +/- 3 g/day during LPD and 81 +/- 4 g/day during UPD (P less than .001). Urinary urea appearance and plasma urea were significantly lower on LPD. Median total urinary protein was reduced from 3.9 g/day (range 0.5-12.3) on UPD to 2.4 (range 0.2-9.0) on LPD (P less than .006), and there was a significant fall in the median fractional clearance of albumin from 2.0 x 10(-4) (range 0.1-90.9) on UPD to 1.0 x 10(-4) (range 0.1-51.4) on LPD and IgG from 2.1 x 10(-5) (range 0.2-238) to 1.5 x 10(-5) (range 0.1-77) (P less than .006 and P less than .02, respectively). The reabsorption rate of beta 2-microglobulin was similar on the two diets and glomerular filtration rate, renal plasma flow, and filtration fraction remained unchanged. Thus, short-term dietary protein restriction reduces diabetic proteinuria independently of blood glucose or systemic blood pressure changes by improving glomerular permselectivity.
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PMID:Renal response to restricted protein intake in diabetic nephropathy. 319 38

In 14 female type I diabetics the influence of preexisting diabetic nephropathy on the behaviour of proteinuria and renal function during and after pregnancy was investigated. We compared albumin and total protein in urine, serum-creatinine, creatinine-clearance, uric acid and beta 2-microglobulin in serum before, during and up to sixth months after pregnancy in 5 diabetic women with preexisting normo-albuminuria, stage II of diabetic nephropathy, in 6 women with microalbuminuria, stage III, and in 3 women with overt proteinuria, stage IV of diabetic nephropathy (by Mogensen); in this last patient-group there was a heavy proteinuria with decreased creatinine clearance and high blood pressure still before the begin of the pregnancy. The albumin- and total protein excretion in urine showed in all diabetic patients a 3- to 8-fold increase during pregnancy and in all cases the increased proteinuria dropped after pregnancy to the preexisting values. A transient nephrotic syndrome in pregnancy developed in 2/6 diabetic women with primary microalbuminuria and in all 3 patients with overt proteinuria, but not in any case of pregnant women with primary normo-albuminuria; the difference between the absolute increase of proteinuria in the 2 patient-groups with stage II and III of diabetic nephropathy was statistically significant (p less than 0.005). The renal function parameters serum-creatinine and creatinine-clearance showed in all pregnant women with stage II or III of diabetic nephropathy the same transient changes as in non-diabetic pregnant women, the mean serum-creatinine concentration showed a decline of 36% respectively 14%, the creatinine clearance an increase of 31% and 36%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in renal protein excretion and kidney function in type I diabetic patients during and following pregnancy in relation to the stage of preexistent diabetic nephropathy]. 343 Oct 31

Seeking to study whether measurement of lysozyme (EC 3.2.1.17) in urine by a reliable radioimmunoassay can provide a suitable index of renal tubular function and how lysozymuria develops in temporal relation to proteinuria in diabetic nephropathy, we have compared the urinary excretion of lysozyme and beta 2-microglobulin with the 15-min excretion rate of phenolsulfonphthalein in 39 patients with Type 2 (non-insulin-dependent) diabetes and investigated the temporal relation between the onset of lysozymuria and proteinuria in 15 patients with Type 1 (insulin-dependent) diabetes. The concentrations of lysozyme and beta 2-microglobulin in urine increased in proportion to the decrease in the rate of excretion of phenolsulfonphthalein in these patients. The coefficient of correlation between lysozyme concentration and the 15-min excretion rate of phenolsulfonphthalein (r = -0.70) was higher than that between beta 2-microglobulin concentration and the 15-min excretion rate of phenolsulfonphthalein (r = -0.46). Abnormally high lysozymuria, suggesting the existence of tubular dysfunction, was demonstrated in six of the patients with Type 1 diabetes who showed no proteinuria or only a slight increase in urinary protein excretion. Lysozymuria may thus be added to a list of the indicators for diabetic nephropathy.
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PMID:Determination of urinary lysozyme for potential detection of tubular dysfunction in diabetic nephropathy. 353 May 28

Urinary excretion of albumin, IgG, and beta 2-microglobulin was examined in 132 (69 men, 63 women) newly diagnosed, middle-aged type II diabetic patients and in 144 (62 men, 82 women) nondiabetic control subjects. Both male (N = 57) and female (N = 29) diabetic patients with normal urinary sediment showed an increased excretion of albumin compared with the respective nondiabetic subjects, and male diabetic patients also had an increased IgG excretion. No consistent difference was found in urinary beta 2-microglobulin concentration between the diabetic and nondiabetic subjects. In all, 19.5% of the diabetic subjects with normal urinary sediment (12 men, 5 women) showed urinary albumin concentration exceeding the highest value (35 mg/24 h) found in nondiabetic subjects without renal disease. The urinary excretion of albumin in the diabetic subjects was not associated with the presence of hypertension or coronary heart disease or with the fasting blood glucose or serum insulin levels measured at diagnosis of diabetes. In male diabetic subjects with urinary albumin excretion greater than 35 mg/24 h, a reduced creatinine clearance was found, suggesting the presence of structural damage associated with diabetic nephropathy. The early increase of urinary albumin excretion in type II diabetic patients may be mostly functional in nature. However, some patients may have structural renal damage associated with diabetic nephropathy present at diagnosis.
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PMID:Proteinuria in newly diagnosed type II diabetic patients. 355 5

Glomerular filtration rate (GFR, single bolus 51Cr-EDTA technique), serum creatinine and serum beta 2-microglobulin concentrations were measured simultaneously in 49 insulin-dependent diabetics with diabetic nephropathy. GFR ranged from 148 to 23 ml/min/1.73 m2. Inverse serum concentrations of creatinine and beta 2-microglobulin showed a significant correlation with GFR over the whole range of values, r = 0.87 and r = 0.90, respectively (p less than 0.001). In the 31 patients with a GFR less than 80 ml/min/1.73 m2, serum concentration of creatinine and beta 2-microglobulin were within the normal range in 12 and 9 patients, respectively. With GFR below 60 ml/min/1.73 m2, all patients had elevated serum beta 2-microglobulin concentrations, while 24% of the patients still had normal creatinine concentration. Linear regression analysis between log GFR and log serum beta 2-microglobulin showed a better relationship than between log GFR and log serum creatinine, slope -0.90 and -0.57, respectively, p less than 0.01. A prospective study for up to 70 months was performed in 18 of the patients. The study showed a closer relationship between the individual rate of decline in log GFR and log serum beta 2-microglobulin compared to log GFR versus log serum creatinine, p less than 0.01. Neither serum creatinine nor serum beta 2-microglobulin can be used as methods for screening of early impairment of renal function (GFR less than 80 ml/min/1.73 m2 in diabetic nephropathy. Our study suggests that serum beta 2-microglobulin is more ideal endogenous marker for GFR estimation than serum creatinine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Monitoring progression of diabetic nephropathy. 389 Mar 16

Serum and urinary beta 2-microglobulin (S-, U-beta 2MG), and creatinine clearance (C-cr) were examined in 41 nephrectomy cases, and changes in glomerular and tubular handling of beta 2MG such as filtered beta 2MG (Fil-beta 2MG), reabsorption of beta 2MG (Reab-beta 2MG) and fractional excretion of beta 2MG (FE-beta 2MG) were studied. Serum creatinine (S-cr) and S-beta 2MG increased significantly after nephrectomy. C-cr decreased immediately after nephrectomy (80%), but recovered up to 87% in 2 to 4 days postoperatively. Fil-beta 2MG decreased immediately after nephrectomy, but increased up to more than the preoperative level in 2 to 4 days postoperatively. On the other hand, Reab-beta 2MG decreased significantly immediately after nephrectomy, and it took 5 to 8 days until recovery. Consequently, urinary excretion of beta 2MG (Ex-beta 2MG) and FE-beta 2MG increased significantly 0 to 4 days postoperatively. These increases in Ex-beta 2MG and FE-beta 2MG were much higher than those seen in diabetic nephropathy, cadmium nephropathy and Cis-diamminedichloroplatinum (II) (CDDP) intoxication, and were not due to drug intoxication such as general anesthesia or antibiotics, but due to glomerulo-tubular unbalance. Clinical data of renal tubular handling of beta 2-microglobulin in cases of interferon therapy or unilateral nephrectomy revealed many interesting aspects of glomerulo-tubular adaptations, and micropuncture study or isolated tubule perfusion study are awaited.
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PMID:[Compensatory changes in beta 2-microglobulin handling in the remnant tubules after contralateral nephrectomy. Observations of beta 2-microglobulin excretion into the urine]. 391 67

A sensitive single measure of diminishing renal function is of importance in attempts to modify the progression of diabetic nephropathy. In 12 insulin-dependent diabetics with proteinuria plasma concentrations of beta 2-microglobulin were found to correlate more closely than plasma creatinine concentrations or creatinine clearance with glomerular function as measured by clearance of 52Cr-EDTA. The plasma beta 2-microglobulin concentration was raised in all patients with diminished glomerular filtration rate (below 80 ml/min/1.73 m2). By contrast, in two of these patients plasma creatinine concentration was normal. Plasma beta 2-microglobulin concentrations were stable throughout the day and not affected by food intake, unlike plasma creatinine concentrations, which rose in the afternoon and evening and after a meat meal. Plasma beta 2-microglobulin concentrations were the same in venous and capillary blood, the capillary blood being readily self-collected. Concentrations of beta 2-microglobulin were stable for up to 24 hours when whole blood was stored at 4 degrees C; adding aprotinin inhibited loss of beta 2-microglobulin for up to seven days. The results of this study suggest, therefore, that measuring beta 2-microglobulin concentrations is a simple and accurate method of detecting minor degrees of renal impairment and monitoring the effects of treatment.
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PMID:Beta 2-microglobulinaemia: a sensitive index of diminishing renal function in diabetics. 616 71

Forty-two patients with renal disease due to diabetic nephropathy (14 patients), tubulointerstitial disease (14 patients) and glomerular disease (14 patients) underwent measurement of glomerular filtration rate (GFR) by the 51Cr-EDTA 'one-shot' method and simultaneous serum beta 2-microglobulin, serum creatinine and creatinine clearance estimation. Serum creatinine was a significantly better predictor of GFR than serum beta 2-microglobulin in patients with diabetic nephropathy, whereas both methods were equally useful predictors of GFR in non-diabetic renal disease. Serum creatinine measurement remains the best method for detecting early reduction of GFR on a serum sample.
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PMID:Predictors of renal function in diabetic and non-diabetic renal disease. 635 17

Nineteen type I diabetic teen-agers without clinical signs of nephropathy with a duration of diabetes varying from 3 to 16.8 years were examined by a standardized exercise test for analysis of urinary excretion of albumin and beta 2-microglobulin. The patients were studied both in poor and improved (but not perfect), metabolic control as defined by HbA1c and blood glucose profiles, and the values were compared to those of 14 age-matched healthy controls. The controls showed no increase in albumin excretion rate during exercise as was found in diabetic patients. The albumin excretion rate during exercise was significantly correlated (p less than 0.05) to systolic blood pressure in the diabetic patients. Blood pressure in the diabetic patients was, however, similar to that of controls both at rest and during exercise. Urinary beta 2-microglobulin did not change during exercise. The urinary albumin excretion during exercise decreased significantly with improved metabolic control in diabetic patients, but the albumin excretion rate was not correlated with either blood or urinary glucose or diuresis during the exercise test. When metabolic control was improved there was a significant correlation between the increase in albumin excretion rate during exercise and the duration of diabetes, indicating that part of the exercise-induced albumin excretion might reflect irreversible morphological changes in the diabetic kidney. This test might therefore have a predictive value for diabetic nephropathy if performed during strict metabolic control.
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PMID:Effect of metabolic control and duration on exercise-induced albuminuria in diabetic teen-agers. 636 69

Glomerular function was monitored prospectively in 13 patients with insulin-dependent diabetes and diabetic nephropathy for up to 51 months. Glomerular filtration rate, measured by 51Cr-EDTA clearance, showed a linear decline in all patients. Rates of fall ranged between 0.63 and 2.4 ml/minute per month (mean +/- SEM 1.2 +/- 0.16). Plasma creatinine concentration proved to be an insensitive marker of glomerular function, especially in the early phase of nephropathy. A good correlation was found between the rate of change of 51Cr-EDTA glomerular filtration rate and that of inverse creatinine levels when plasma creatinine concentrations exceeded 200 mumol/liter. Inverse plasma beta 2-microglobulin concentrations, however, showed a highly significant correlation (r = 0.93; p less than 0.001) with 51Cr-EDTA glomerular filtration rate over the whole range of values, making it sensitive in screening for early impairment of renal function. A significant relationship (r = 0.85; p less than 0.01) was found between the rates of change of the 51Cr-EDTA glomerular filtration rate and of inverse beta 2-microglobulin levels for plasma beta 2-microglobulin concentrations above 3 mg/liter. A progressive increase in the fractional clearance of albumin, IgG, and beta 2-microglobulin was noted as the glomerular filtration rate fell, indicating an evolving defect in the renal handling of proteins. The rate of decline of the glomerular filtration rate was unrelated to age, sex, duration of diabetes, duration of diabetes before onset of proteinuria, glomerular filtration rate, initial albumin clearance, blood glucose control, and arterial pressure, when diastolic values were below 100 mm Hg. The effect of therapeutic intervention (e.g., blood glucose, blood pressure, or diet) on the progression of diabetic nephropathy can be reliably evaluated by precise measures of rate of decline of glomerular filtration rate and changes in fractional clearance of plasma proteins. The factor(s) determining the individual rate of decline of renal function still remain obscure.
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PMID:Monitoring glomerular function in diabetic nephropathy. A prospective study. 640 24


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